Please note that data concerning SLPI expression in these

Please note that data concerning SLPI expression in these cohorts were published previously, therefore these data are not shown in detail in this study. As illustrated in figure 2, a significant positive correlation was identified in eradicated subjects, whereas no correlation was seen in both other groups as well as in the combined data set. No correlations between Progranulin and SLPI were identified in corpus mucosa and serum of the three indi vidual groups. Immunohistochemical localization of Progranulin in the gastric mucosa As illustrated in figure 3, both epithelial and infiltrating immune cells contribute to the mucosal Progranulin expression. Immune cells showed constantly high expression of Progranulin except cells of lymphoid follicles. Higher numbers of Progranu lin expressing cells were associated with gastritis in H.

pylori infected subjects. For the epithelium, strongest expression was observed in the gastric glands followed by the basis of the foveolae mainly in areas of dense inflammatory infiltrate. Surface epithelium between gastric pits showed weak or no expression of Progranulin. Semiquantitative scoring revealed significant higher expression scores of Progranulin for H. pylori infected subjects compared to both other groups in antrum, whereas a tendency was observed for corpus. Furthermore, the number of infiltrating Progranulin expressing immune cells was significantly higher in both antral and corpus mucosa of H. pylori infected subjects. Expression of Progranulin and SLPI in epithelial AGS cells infected by H.

pylori To investigate the regulatory link between SLPI and Progranulin, both molecules were investigated in rela tion to H. pylori infection and siRNA mediated downre gulation of SLPI expression in AGS cells. As demonstrated in figure 5, cellular SLPI levels were sig nificantly reduced by 33%, 63%, and 81. 3% by H. pylori, siRNA, and both factors, respectively. SLPI levels in the supernatant were strongly reduced by siRNA, but not by H. pylori. The analysis of Progranulin levels in the identical samples, revealed no effect of SLPIsiRNA treatment. Both cellular as well as secreted Progranulin levels were similar to those of controls. H. pylori infection was asso ciated with elevated Progranulin level in supernatant, while cellular levels were found to be slightly reduced. The combined effect of H.

pylori and SLPI siRNA approach resulted in similar changes. Discussion Here we demonstrate that the H. pylori infection is associated with increased Progranulin levels in the antrum of infected subjects, and that both epithelial and infil trating immune cells contribute to this phenomenon. Furthermore, we provided evidence that the upregula Entinostat tion of Progranulin seems to be independent of SLPI levels. Considering the central role of the elastase SLPI equilibrium for the conversion of Progranulin to granulins and the previously identified deregulation of elastase SLPI expression in H.

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